Excess secretion of acid in the stomach is one of the important factors which cause peptic ulcers. Because of this, administration of drugs which neutralize the acid or inhibit secretion of the acid is used for the treatment of peptic ulcers.
For example, sodium bicarbonate, magnesium oxide and the like are clinically used as antacids which neutralize the acid. Such antacids, however, are a burden to patients because of the necessity of frequent administration, and they also have side effects such as alkalosis and the like. On the other hand, anticholinergics such as atropine, pirenzepine and the like are used clinically as acid secretion inhibitors. However, such anticholinergics are not necessarily high in the selectivity for gastric acid secretion and cause side effects such as thirst, visual acuity disorder, urinary retention, tachycardia and the like. Also used clinically as acid secretion inhibitors are histamine H.sub.2 -receptor antagonists such as cimetidine, ranitidine, famotidine and the like. However, these histamine H.sub.2 -receptor antagonists are not effective in healing certain types of intractable ulcer and it is also pointed out that these antagonists cause side effects such as milk secretion due to increased blood prolactin level, gynecomastia induced by anti-androgen reaction and inhibition of the metabolism of other drugs in the liver.
Recently, proton pump inhibitors, such as omeprazole, which inhibit proton pump functioning in the final stage of the gastric acid secretion are clinically used and resulting in an efficacy similar to or higher than that of histamine H.sub.2 -receptor antagonists. In addition, since the proton pump functions in the final stage of the acid secretion, these proton pump inhibitors are also effective on histamine-independent gastric acid secretion and therefore partially effective in healing intractable ulcers which cannot be healed by histamine H.sub.2 -receptor antagonists.
However, since peptic ulcers are apt to relapse, they can be healed but their relapse can hardly be avoided even by the use of these histamine H.sub.2 -receptor antagonists or proton pump inhibitors. The following is considered to be one of the reason for this problem. That is, in the normal stomach, gastric acid and gastric mucosa defense mechanism keep balance with each other so that the stomach is not damaged by the acid secreted by itself. However, such a balance is lost and a peptic ulcer is generated when excess secretion of the acid occurs or function of the gastric mucosa defense mechanism is reduced. When a histamine H.sub.2 -receptor antagonist or a proton pump inhibitor is administered as a therapeutic drug of the peptic ulcer, secretion of the acid decreases so that it becomes unnecessary to control the gastric mucosa defense mechanism at similar level to that before the drug administration. Because of this, the function of the gastric mucosa defense mechanism is reduced when the peptic ulcer is healed and the drug administration becomes unnecessary. In consequence, when administration of the histamine H.sub.2 -receptor antagonist or proton pump inhibitor is terminated under such conditions, the acid secretion quantity quickly returns to the level prior to the drug administration, but the gastric mucosa defense mechanism is not restored quickly to its normal state, thus putting the gastric acid and the gastric mucosa defense mechanism out of balance and relapsing of the peptic ulcer.
Under such circumstances described above, great concern has been directed toward the development of a therapeutic agent having a broad range of efficacy, namely a drug for use in the prevention and/or treatment of peptic ulcer-related diseases, which is effective on intractable ulcers that cannot be healed by the prior art drugs and which can prevent relapse of ulcers.